PKA mediates the effects of monoamine transmitters on the K+ current underlying the slow spike frequency adaptation in hippocampal neurons. Export

@article{citeulike:715468, abstract = {The Ca(2+)-activated K+ current IAHP, which underlies spike frequency adaptation in cortical pyramidal cells, can be modulated by multiple transmitters and probably contributes to state control of the forebrain by ascending monoaminergic fibers. Here, we show that the modulation of this current by norepinephrine, serotonin, and histamine is mediated by protein kinase A in hippocampal CA1 neurons. Two specific protein kinase A inhibitors, Rp-cAMPS and Walsh peptide, suppressed the effects of these transmitters on IAHP and spike frequency adaptation. The effects of the cyclic AMP analog 8CPT-cAMP were also inhibited, whereas muscarinic and metabotropic glutamate receptor agonists had full effect. Intracellular application of protein kinase A catalytic subunit or a phosphatase inhibitor mimicked the effects of monoamines or 8CPT-cAMP. These results demonstrate that monoaminergic modulation of neuronal excitability in the mammalian CNS is mediated by protein phosphorylation.}, address = {Institute of Neurophysiology, University of Oslo, Norway.}, author = {Pedarzani, P. and Storm, J. F.}, citeulike-article-id = {715468}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/8274274}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=8274274}, issn = {0896-6273}, journal = {Neuron}, keywords = {bar, ca1, pka}, month = {December}, number = {6}, pages = {1023--1035}, posted-at = {2006-06-29 10:03:10}, priority = {4}, title = {PKA mediates the effects of monoamine transmitters on the K+ current underlying the slow spike frequency adaptation in hippocampal neurons.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/8274274}, volume = {11}, year = {1993} }

TY - JOUR ID - citeulike:715468 L3 - citeulike-article-id:715468 N2 - The Ca(2+)-activated K+ current IAHP, which underlies spike frequency adaptation in cortical pyramidal cells, can be modulated by multiple transmitters and probably contributes to state control of the forebrain by ascending monoaminergic fibers. Here, we show that the modulation of this current by norepinephrine, serotonin, and histamine is mediated by protein kinase A in hippocampal CA1 neurons. Two specific protein kinase A inhibitors, Rp-cAMPS and Walsh peptide, suppressed the effects of these transmitters on IAHP and spike frequency adaptation. The effects of the cyclic AMP analog 8CPT-cAMP were also inhibited, whereas muscarinic and metabotropic glutamate receptor agonists had full effect. Intracellular application of protein kinase A catalytic subunit or a phosphatase inhibitor mimicked the effects of monoamines or 8CPT-cAMP. These results demonstrate that monoaminergic modulation of neuronal excitability in the mammalian CNS is mediated by protein phosphorylation. IS - 6 JF - Neuron SN - 0896-6273 AD - Institute of Neurophysiology, University of Oslo, Norway. EP - 1035 TI - PKA mediates the effects of monoamine transmitters on the K+ current underlying the slow spike frequency adaptation in hippocampal neurons. VL - 11 SP - 1023 KW - bar KW - ca1 KW - pka AU - Pedarzani, P AU - Storm, JF PY - 1993/12// UR - http://view.ncbi.nlm.nih.gov/pubmed/8274274 ER -